Cardiovascular disease (CVD) risk is highest in developed nations, and the reasons may include high psychological stress and insufficient sleep, each of which increases systemic inflammation and impairs vascular health. Arterial stiffness (AS), a vascular property that worsens with chronic inflammation, has emerged as an early, independent predictor of CVD risk, providing prognostic information beyond standard models that include blood pressure. Our preliminary data suggest that a) objectively assessed sleep is inversely associated with AS; b) ecological momentary assessed (EMA) stress dynamically increases AS; and, c) those with a greater AS response to laboratory stress have higher 24hr average AS. These pilot data are evidence that high real world AS may be due to both repeated instances of ?arterial stiffening? during stress and to overall insufficient sleep. We propose to utilize both field and controlled laboratory methods to determine, 1) the effect of EMA psychological stress on momentary AS; 2) the effect of actigraphy-assessed sleep duration on AS; and 3) the acute effects of partial sleep deprivation (PSD) on next day AS, and on the AS response to psychological stress under controlled conditions. Field: 300 healthy adults will complete 7- days of actigraphy-assessed sleep that will include a single night assessment of sleep disordered breathing. For the 6th day/night and 7th day of assessment (36hrs), ambulatory AS with concurrent EMA of psychological stress, physical activity, and related factors will be accomplished every 60 minutes. Lab: 132 of these individuals who demonstrate 6.5-8.9 hrs actigraphy-assessed sleep/night for at least 5-7 nights will spend 2 days in the CRC (acclimation night, baseline sleep night, PSD night). On the morning after baseline and PSD nights, they will complete a psychological stress protocol under controlled laboratory conditions. Field Study - Hypothesis 1a: EMA assessed psychological stress will predict momentary AS; and Hypothesis 1b: actigraphy-assessed sleep duration will predict both, i) the average daytime AS and, ii) the AS response to EMA assessed psychological stress. We will explore the effect of average psychological stress and average sleep duration on average daytime and nocturnal AS, and AS dipping. Laboratory Study - Hypothesis 2: Compared to baseline sleep, PSD will be associated with a) higher next day AS, and b) a greater AS response to laboratory psychological stress. We will explore the relationship of inflammation to both resting AS and laboratory stress-related changes in AS, as a possible mechanism through which stress and sleep affect AS. Significance: Increasing stress and decreasing sleep are two modifiable factors endemic to developed nations where CVD risk is highest. AS has emerged as an early, independent predictor of CVD risk. The proposed study will provide a strong test of hypothesized effects on AS due to stress and sleep, thereby providing powerful targets for interventions such as stress management, sleep hygiene, and cognitive behavioral therapy for insomnia, to delay AS onset, and improve CV outcomes.